Background. Empathy plays a key role in social understanding, but its empirical measurement has proved difficult. The Empathy Quotient (EQ) is a self-report scale designed to do just that. This series of four studies examined the reliability and validity of the EQ and determined its factor structure.

Depersonalisation disorder is a recognisable clinical entity but appears to have significant comorbidity with anxiety and depression. Research into its aetiology and treatment is warranted.

Developing protein therapeutics has posed challenges due to short circulating times and toxicities. Recent advances using poly(ethylene) glycol (PEG) conjugation have improved their performance. A PEG-conjugated hemoglobin (Hb), Hemospan, is in clinical trials as an oxygen therapeutic. Solutions of PEG-hemoglobin with two (P5K2) or six to seven strands of 5-kD PEG (P5K6) were studied by small-angle x-ray scattering. PEGylation elongates the dimensions (Hb < P5K2 < P5K6) and leaves the tertiary hemoglobin structure unchanged but compacts its quaternary structure. The major part of the PEG chains visualized by ab initio reconstruction protrudes away from hemoglobin, whereas the rest interacts with the protein. PEGylation introduces intermolecular repulsion, increasing with conjugated PEG amount. These results demonstrate how PEG surface shielding and intermolecular repulsion may prolong intravascular retention and lack of reactivity of PEG-Hb, possibly by inhibiting binding to the macrophage CD163 hemoglobin-scavenger receptor. The proposed methodology for assessment of low-resolution structures and interactions is a powerful means for rational design of PEGylated therapeutic agents.

Symptoms of depersonalization belong to distinct but related psychopathological domains.

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DNA double-stranded breaks (DSBs) are among the most severe forms of DNA damage and responsible for chromosomal translocations that may lead to gene fusions. The RAD51 family plays an integral role in preserving genome stability by homology directed repair of DSBs. From a proteomics screen, we recently identified SFPQ/PSF as an interacting partner with the RAD51 paralogs, RAD51D, RAD51C and XRCC2. Initially discovered as a potential RNA splicing factor, SFPQ was later shown to have homologous recombination and non-homologous end joining related activities and also to bind and modulate the function of RAD51. Here, we demonstrate that SFPQ interacts directly with RAD51D and that deficiency of both proteins confers a severe loss of cell viability, indicating a synthetic lethal relationship. Surprisingly, deficiency of SFPQ alone also leads to sister chromatid cohesion defects and chromosome instability. In addition, SFPQ was demonstrated to mediate homology directed DNA repair and DNA damage response resulting from DNA crosslinking agents, alkylating agents and camptothecin. Taken together, these data indicate that SFPQ association with the RAD51 protein complex is essential for homologous recombination repair of DNA damage and maintaining genome integrity.

Depersonalisation disorder involves an unpleasant, chronic and disabling alteration in the experience of self and environment. In addition to these classic features of depersonalisation and derealisation, symptoms may also encompass alterations in bodily sensation and a loss of emotional reactivity. Primary depersonalisation disorder is probably more common than previously thought, and here we discuss the diagnosis, assessment and treatment of the condition, with particular reference to our experiences in a specialist depersonalisation clinic. We also consider psychological and biological aspects of the condition. Although there is as yet no recognised treatment for this disorder, various pharmacological interventions, particularly a combination of lamotrigine and a selective serotonin reuptake inhibitor, have shown promise. We discuss these drug treatments, together with psychological approaches, in particular a recent cognitive–behavioural conceptualisation and treatment approach.

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